product name Dutasteride
Description: Dutasteride (also known as GI198745, GG-745) is a dual 5-α reductase inhibitor that inhibits conversion of testosterone to dihydrotestosterone (DHT). Dutasteride inhibited conversion of 3H-testosterone to 3H-DHT by more than 99% in LNCaP cells.It can also strongly reduces growth, proliferation, and viability of LNCaP cells as well. Dutasteride increased the enzymatic activities of caspase 7 and caspase 8 dose-dependently at 48 hours, providing functional significance and confirming that the apoptotic and survival pathways are being activated by dutasteride treatment in LNCaP cells.
References: Curr Top Med Chem. 2006;6(5):405-21.
528.53
Formula
C27H30F6N2O2
CAS No.
164656-23-9
Storage
-20℃ for 3 years in powder form
-80℃ for 2 years in solvent
Solubility (In vitro)
DMSO: 62 mg/mL (117.3 mM)
Water: <1 mg/mL
Ethanol: 6 mg/mL (11.4 mM)
Solubility (In vivo)
Synonyms
GI198745, GG-745
other peoduct :References PubMed ID：:http://www.ncbi.nlm.nih.gov/pubmed/19399829
| In Vitro |
In vitro activity: Dutasteride inhibits type-1 5AR and type-2 5AR with IC50 of 6 nM and 7 nM, respectively. Dutasteride is 60-fold more potent than Finasteride in its initial Ki versus type 1 5AR and ~5-fold more rapid in inactivating the enzyme. Dutasteride inhibits (3)H-T conversion to (3)H-DHT and, as anticipated, inhibits T-induced secretion of PSA and proliferation in LNCaP cells. Dutasteride also inhibits DHT-induced PSA secretion and cell proliferation with IC50 of 1 μM in LNCaP cells. Dutasteride competes for binding the LNCaP cell AR with an IC50 of 1.5 μM. Dutasteride (10–50 μM) results in enhanced cell death, possibly by apoptosis, in steroid-free medium. Dutasteride reduces cell viability and cell proliferation in androgen-responsive (LNCaP) and androgen-unresponsive (DU145) human prostate cancer(PCa) cell lines. Dutasteride results in overexpressed genes included genes encoding for proteins involved in biosynthesis and metabolism of androgen (HSD17B1;HSD17B3;CYP11B2), androgen receptor and androgen receptor co-regulators (AR;CCND1), and signal transduction(ERBB2; V-CAM; SOS1) whereas, underexpressed genes (KLK3; KLK2; DHCR24) are androgen-regulated genes (ARGs) in androgen-responsive (LNCaP) cell. Dutasteride inhibits FASN mRNA, protein expression and enzymatic activity in prostate cancer cells. Kinase Assay: Cell Assay: Dutasteride has been reported to inhibit conversion of 3H-testosterone to 3H-DHT by more than 99% in LNCaP cells. Dutasteride strongly reduces growth, proliferation, and viability of LNCaP cells as well. Dutasteride increased the enzymatic activities of caspase 7 and caspase 8 dose-dependently at 48 hours, providing functional significance and confirming that the apoptotic and survival pathways are being activated by dutasteride treatment in LNCaP cells. |
|---|---|
| In Vivo | Dutasteride (100 mg/kg/day) has prostates about half as large as those in intact male rats treated with vehicle alone. Dutasteride is orally bioavailable and because of its mechanism of action it easily overcomes the potential liability of being >99% plasma protein bound. |
| Animal model | |
| Formulation & Dosage | |
| References | Curr Top Med Chem. 2006;6(5):405-21. |
Related Posts
product name Dutasteride
Description: Dutasteride (also known as GI198745, GG-745) is a dual 5-α reductase inhibitor that inhibits conversion of testosterone to dihydrotestosterone (DHT). Dutasteride inhibited conversion of 3H-testosterone to 3H-DHT by more than 99% in LNCaP cells.It can also strongly reduces growth, proliferation, and viability of LNCaP cells as well. Dutasteride increased the enzymatic activities of caspase 7 and caspase 8 dose-dependently at 48 hours, providing functional significance and confirming that the apoptotic and survival pathways are being activated by dutasteride treatment in LNCaP cells.
References: Curr Top Med Chem. 2006;6(5):405-21.
528.53
Formula
C27H30F6N2O2
CAS No.
164656-23-9
Storage
-20℃ for 3 years in powder form
-80℃ for 2 years in solvent
Solubility (In vitro)
DMSO: 62 mg/mL (117.3 mM)
Water: <1 mg/mL
Ethanol: 6 mg/mL (11.4 mM)
Solubility (In vivo)
Synonyms
GI198745, GG-745
other peoduct :References PubMed ID：:http://www.ncbi.nlm.nih.gov/pubmed/19399829
| In Vitro |
In vitro activity: Dutasteride inhibits type-1 5AR and type-2 5AR with IC50 of 6 nM and 7 nM, respectively. Dutasteride is 60-fold more potent than Finasteride in its initial Ki versus type 1 5AR and ~5-fold more rapid in inactivating the enzyme. Dutasteride inhibits (3)H-T conversion to (3)H-DHT and, as anticipated, inhibits T-induced secretion of PSA and proliferation in LNCaP cells. Dutasteride also inhibits DHT-induced PSA secretion and cell proliferation with IC50 of 1 μM in LNCaP cells. Dutasteride competes for binding the LNCaP cell AR with an IC50 of 1.5 μM. Dutasteride (10–50 μM) results in enhanced cell death, possibly by apoptosis, in steroid-free medium. Dutasteride reduces cell viability and cell proliferation in androgen-responsive (LNCaP) and androgen-unresponsive (DU145) human prostate cancer(PCa) cell lines. Dutasteride results in overexpressed genes included genes encoding for proteins involved in biosynthesis and metabolism of androgen (HSD17B1;HSD17B3;CYP11B2), androgen receptor and androgen receptor co-regulators (AR;CCND1), and signal transduction(ERBB2; V-CAM; SOS1) whereas, underexpressed genes (KLK3; KLK2; DHCR24) are androgen-regulated genes (ARGs) in androgen-responsive (LNCaP) cell. Dutasteride inhibits FASN mRNA, protein expression and enzymatic activity in prostate cancer cells. Kinase Assay: Cell Assay: Dutasteride has been reported to inhibit conversion of 3H-testosterone to 3H-DHT by more than 99% in LNCaP cells. Dutasteride strongly reduces growth, proliferation, and viability of LNCaP cells as well. Dutasteride increased the enzymatic activities of caspase 7 and caspase 8 dose-dependently at 48 hours, providing functional significance and confirming that the apoptotic and survival pathways are being activated by dutasteride treatment in LNCaP cells. |
|---|---|
| In Vivo | Dutasteride (100 mg/kg/day) has prostates about half as large as those in intact male rats treated with vehicle alone. Dutasteride is orally bioavailable and because of its mechanism of action it easily overcomes the potential liability of being >99% plasma protein bound. |
| Animal model | |
| Formulation & Dosage | |
| References | Curr Top Med Chem. 2006;6(5):405-21. |